Pseudomonas aeruginosa bacteriophage phi PLS27-lipopolysaccharide interactions.
We investigated the phi PLS27 receptor in Pseudomonas aeruginosa strain PAO lipopolysaccharide (LPS) by analyzing a resistant mutant. This mutant, which was designated AK1282, had the most defective LPS yet reported for a P. aeruginosa rough mutant; this LPS contained only lipid A, 2-keto-3-deoxyoctonate, heptose, and alanine as major components. In addition, this LPS lacked galactosamine, which is present in the inner core of the LPS of other rough mutants. The loss of galactosamine but only a small decrease in the alanine content indicated that the core of strain PAO LPS differed from the core structure which has been suggested for the LPS of other well-characterized P. aeruginosa strains. Our analysis also indicated that galactosamine residues may be crucial for phi PLS27 receptor activity of the LPS. Electrodialysis of LPS and conversion to salt forms (sodium or triethylamine) influenced the phage-inactivating capacity of the LPS, as did the medium in which the inactivation occurred; experiments performed in 1/10-strength broth resulted in much lower PhI50 (concentration of LPS causing a 50% decrease in the titer of phage during 1 h of incubation at 37 degrees C) values than experiments performed in regular-strength broth. Sonication of the LPS also increased the phage-inactivating capacities of the LPS preparations.
D001435:Bacteriophages / Q000502:physiology*; D002412:Cations / Q000032:analysis; D005688:Galactosamine / Q000502:physiology; D008070:Lipopolysaccharides / Q000032:analysis / Q000494:pharmacology / Q000502:physiology*; D011550:Pseudomonas aeruginosa / Q000032:analysis*; D011991:Receptors, Virus / Q000032:analysis / Q000502:physiology*; D013010:Sonication
D002412:Cations; D008070:Lipopolysaccharides; D011991:Receptors, Virus; D005688:Galactosamine